Inhibitory effect of porphyran on lipopolysaccharide-induced activation of human immune cells

• Published in: Carbohydrate polymers Vol. 232; p. 115811
• Main Authors: Wang, Yuhua, Hwang, Juyoung, Yadav, Dhananjay, Oda, Tatsuya, Lee, Peter Chang-Whan, Jin, Jun-O
• Format: Journal Article
• Language: English
• Published: England Elsevier Ltd 15.03.2020
• Subjects: Anti-Inflammation; Human peripheral blood dendritic cell; Human peripheral blood mononuclear cell; Lipopolysaccharide; Porphyran; Ab; TCR; IL; MODC; DAPI; PBMC; Porphyran; LPS; mAb; IFN; RBC; PBDC; Human peripheral blood mononuclear cell; GM-CSF; Lipopolysaccharide; MD2; SEM; CCR7; Anti-Inflammation; TLR; Human peripheral blood dendritic cell; DC
• ISSN: 0144-8617; 1879-1344
• DOI: 10.1016/j.carbpol.2019.115811

•Pyropia yezoensis porphyran inhibits LPS-induced proinflammatory cytokines in human PBMCs.•Porphyran suppresses LPS-induced human MODC and PBDC activation.•LPS binding to TLR4/MD2 complex is interrupted by porphyran in human PBDCs. In mice, porphyran extracted from Pyropia yezoensis exerts anti-inflammatory effects and suppresses lipopolysaccharide (LPS)-induced immune activation and sepsis. Here, we investigated inhibition of LPS-induced activation of human immune cells by porphyran and the underlying mechanisms. We demonstrated that porphyran may inhibit LPS-induced proinflammatory cytokine production in peripheral blood mononuclear cells, monocyte-derived dendritic cells, and peripheral blood dendritic cells. We also observed that porphyran-mediated LPS-induced activation of DC suppressed syngeneic T cell proliferation, resulting in reduced production of interferon-γ. The mechanism of LPS-induced immune cell activation requires the activation of toll like receptor 4 following binding of LPS to myeloid differentiation factor 2 (MD2). Additionally, we show that porphyran competes with LPS for binding to MD2 and thereby suppresses immune cell activation. Porphyran may, therefore, be a promising therapeutic candidate for the treatment of endotoxin-mediated septic shock and inflammation in humans.